1. Field of the Invention
The invention relates to a method and composition for the treatment of obesity. In particular, the invention relates to a method for reducing overall caloric intake comprising administering a nutritive food supplement which inhibits feeding and elicits satiety through established hormonal and neural feedback mechanisms.
2. Prior Art
The failure to control food intake in a normal manner has long been thought to be a major cause of obesity. A lack of understanding of the control mechanisms by which food intake is regulated in the normal animal or human has, however, prevented an effective clinical application of this concept.
Until quite recently, the primary physiological appetite control mechanisms were generally believed to be stimulated by an increase in blood glucose levels and/or gastric distension resulting from food intake. It is now postulated that these appetite controls are of secondary importance, and that a primary mechanism for eliciting satiety and inhibiting feeding comprises the release of peptide hormones in the small intestine on preabsorptive contact of food stimuli with mucosal gut receptors; while a number of peptide hormones may participate, the "satiety effect" (appetite suppression) of cholecystokinin (CCK) appears at this time to be particularly significant. An elaboration of the investigatory work on this hormone and a proposed elucidation of its role as an appetite suppressant is presented by G. P. Smith in Biochemical Pharmacology of Obesity, pp. 407-419 (Elsevier Science Publishers, 1983).
The recognition of the physiological activity of CCK and related hormones in the eliciting of satiety was followed by a recognition of the therapeutic potential of these hormones by Smith and others: Saito et al, Science 208: 1155-1156, 1980; Della-Fera et al, Physiol. Behavior 24: 943-950, 1980; Gibbs et al. Nature 282: 208-210, 1979; Malaisse-Lagae et al, Experientia 33: 915-917, 1977; Smith et al: In D. Novin et al (Eds.) Hunger-Basic Mechanisms and Clinical Implications, Raven, N.Y., pp. 349-355, 1976; Gibbs et al., Am. J. Physiol 230: 15-18, 1976; Fincham et al, Program, 6th Int. Conf. Phys. of Food and Fluid Intake, 1977; Meyer et al. Am. J. Physiol. 222: 1058-1063, 1972. Clinical applications of particular interest appear to include both the exogenous administration or inducement of endogenous release of gut peptides such as CCK. In particular, the administration of a chemical stimulus to the release of the hormone(s) of interest has been proposed, including the use of L-phenylalanine as a preabsorptive releaser of CCK (Fincham, Program, supra). It is, however, recognized (e.g., Smith, G. P., Biochemical Pharmacology of Obesity, supra) that the mere clinical administration of these peptides, or the clinical initiation of their release, is not, per se, an adequate treatment for obesity. [cf. Gibbs et al, Am. J. Physiol. 230: 15-18,17(1976), Smith et al, Hunger-Basic Mechanisms, supra., p. 353.]